Zinc(II) ion promotes anti-inflammatory effects of rhSOD3 by increasing cellular association.

Zinc(II) ion promotes anti-inflammatory effects of rhSOD3 by increasing cellular association.
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DOI:
10.5483/bmbrep.2017.50.2.150
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发表时间:
2017-02
期刊:
影响因子:
3.8
通讯作者:
Kim TY
Kim TY
中科院分区:
生物学3区
文献类型:
--
作者:
Kim Y;Jeon YJ;Ryu K;Kim TY

文献摘要

被引文献

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最近,我们证明了超氧化物歧化酶3 (SOD3)是一个强有力的候选生物医学。SOD3的抗氧化功能是在没有细胞渗透的情况下完成的,它通过非酶功能抑制炎症反应。SOD3具有与细胞表面相关的肝素结合域。有趣的是,我们发现Zn2+通过增加肝素结合域(HBD)的摄取来促进重组人SOD3 (rhSOD3)的转导作用。我们证明了通过HBD从培养基中摄取rhSOD3到细胞裂解液,导致细胞核中rhSOD3的积累,这是由Zn2+的存在促进的。这导致在Zn2+存在下,rhSOD3对NF-kB和STAT3信号的抑制作用增强,这表明rhSOD3与细胞的关联升高。这些结果表明,优化的程序可以帮助增强rhSOD3作为一种新型生物药物的炎症疗效。
Recently, we demonstrated that superoxide dismutase 3 (SOD3) is a strong candidate for biomedicine. Anti-oxidant function of SOD3 was accomplished without cell penetration, and it inhibited the inflammatory responses via non-enzymatic functions. SOD3 has the heparin binding domain associating cell surface. Interestingly, we found that Zn2+ promotes transduction effects of recombinant human SOD3 (rhSOD3) by increasing uptake via the heparin binding domain (HBD). We demonstrated an uptake of rhSOD3 from media to cell lysate via HBD, resulting in an accumulation of rhSOD3 in the nucleus, which was promoted by the presence of Zn2+. This resulted in increased inhibitory effects of rhSOD3 on NF-kB and STAT3 signals in the presence of Zn2+, which shows elevated association of rhSOD3 into the cells. These results suggest that an optimized procedure can help to enhance the inflammatory efficacy of rhSOD3, as a novel biomedicine.